Y
Ying Xia
Researcher at Fudan University
Publications - 223
Citations - 10897
Ying Xia is an academic researcher from Fudan University. The author has contributed to research in topics: Neuroprotection & Receptor. The author has an hindex of 50, co-authored 210 publications receiving 9897 citations. Previous affiliations of Ying Xia include La Jolla Institute for Allergy and Immunology & University of California, San Diego.
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Journal ArticleDOI
Signaling by proinflammatory cytokines: oligomerization of TRAF2 and TRAF6 is sufficient for JNK and IKK activation and target gene induction via an amino-terminal effector domain.
TL;DR: Oligomerization of the TRAF2 effector domain results in specific binding to MEKK1, a protein kinase capable of JNK, p38, and IKK activation, and induction of TNF-alpha and IL-1 responsive genes.
Journal ArticleDOI
Jun Turnover Is Controlled Through JNK-Dependent Phosphorylation of the E3 Ligase Itch
Min Gao,Tord Labuda,Tord Labuda,Tord Labuda,Ying Xia,Ying Xia,Ying Xia,Ewen Gallagher,Ewen Gallagher,Ewen Gallagher,Deyu Fang,Deyu Fang,Deyu Fang,Yun Cai Liu,Yun Cai Liu,Yun Cai Liu,Michael Karin,Michael Karin,Michael Karin +18 more
TL;DR: It is found that extracellular stimuli also modulate protein turnover by regulating the activity of an E3 ligase by means of its phosphorylation.
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Hypoxia-enhanced wound-healing function of adipose-derived stem cells: increase in stem cell proliferation and up-regulation of VEGF and bFGF.
Eun Young Lee,Ying Xia,Won Serk Kim,Myoung Hee Kim,Tae-Hwan Kim,Kea Jeung Kim,Byung Soon Park,Jong Hyuk Sung +7 more
TL;DR: Results suggest that hypoxia increases the proliferation of ADSC and enhances the wound‐healing function of ADSCs, at least partly, by up‐regulating the secretion of VEGF and bFGF.
Journal ArticleDOI
Mechanisms underlying hypoxia-induced neuronal apoptosis
TL;DR: The known mechanisms underlying apoptosis in neurons exposed to Hypoxia and hypoxia-ischemia are examined and it is suggested that the balance in the expression of pro- and anti-apoptotic genes that likely determines the fate of neurons exposure to hypoxIA may also account for the regional differences in vulnerability to hypoxic insults.
Journal ArticleDOI
MEK kinase 1 is critically required for c-Jun N-terminal kinase activation by proinflammatory stimuli and growth factor-induced cell migration.
TL;DR: Using MEKK1-deficient embryonic stem cells prepared by gene targeting, the function of the MAP3K MEK kinase 1 (MEKK1) in proinflammatory signaling is examined and it is found that it is required for JNK activation by diverse proinflammatory stimuli, including tumor necrosis factor alpha, IL-1, double-stranded RNA, and lipopolysaccharide.